Coudon W L, Harris J O
Chest. 1978 Mar;73(3):364-70. doi: 10.1378/chest.73.3.364.
The occurrence of emphysema in people deficient in alpha1-antitrypsin and the production of emphysema in experimental animals with elastolytic enzymes suggest proteolysis as a mechanism for the development of emphysema. To investigate the possible role of pulmonary alveolar macrophages in the pathogenesis of emphysema, we measured elastase, acid protease, and elastase-like esterase activities in macrophages from patients with chronic obstructive lung disease and attempted to correlate the level of enzyme activity with the severity of pulmonary function abnormality measured in these patients. Compared to values for cigarette smokers with normal pulmonary function, these macrophage enzyme activities were not increased in patients with chronic obstructive lung disease, and there was no correlation of high elastase activity with more severe degrees of pulmonary function abnormality. These findings lead us to believe that the absolute level of proteolytic enzymes in pulmonary alveolar macrophages is not in itself a determinant of emphysema.
α1 -抗胰蛋白酶缺乏的人群中出现肺气肿，以及用弹性蛋白酶处理的实验动物产生肺气肿，这表明蛋白水解作用是肺气肿发生发展的一种机制。为了研究肺泡巨噬细胞在肺气肿发病机制中可能发挥的作用，我们检测了慢性阻塞性肺疾病患者巨噬细胞中的弹性蛋白酶、酸性蛋白酶和弹性蛋白酶样酯酶活性，并试图将酶活性水平与这些患者肺功能异常的严重程度相关联。与肺功能正常的吸烟者相比，慢性阻塞性肺疾病患者的这些巨噬细胞酶活性并未增加，且弹性蛋白酶活性高与更严重程度的肺功能异常之间没有相关性。这些发现使我们相信，肺泡巨噬细胞中蛋白水解酶的绝对水平本身并非肺气肿的决定因素。
